Background:The effect of chronic parenteral infusions of either saline (S), dextrose (D), amino acids without glutamine (AA), or amino acids including glutamine dipeptides (AA+GLN) on interorgan movement of glutamine (GLN) and glutamate (GLU) after fasting was examined.Methods:Multicatheterized mongrel dogs were stressed by fasting for 4 days followed by a 4‐day IV infusion of either S (30 mL/h, n = 8), D (8.6 kcal/h, n = 8), isocaloric AA (8.3 g N/d, n = 7), or isocaloric AA+GLN (8.3 g N/d, 6.8 g GLN/d, n = 6). Hepatic and hindlimb blood flows were estimated, and net arterio‐venous balance measurements (μLmol/kg per minute) were made during the last 2 hours of infusion.Results:Arterial blood concentrations of GLU were 47 ± 6, 52 ± 3, 47 ± 5, and 62 ± 8 and of GLN were 587 ± 25, 548 ± 20, 423 ± 22 (p≤.05vsS), and 512 ± 59 μmol/L for S, D, AA, and AA+GLN, respectively. Slight GLU uptake and GLN release by the hindlimb were observed in all groups. Gut GLU production was ‐0.31 ± 0.06, ‐0.04 ± 0.07 (p≤.05vsS), ‐0.15 ± 0.05, and ‐0.14 ± 0.02 (p≤.05vsS), and gut GLN uptake was 0.64 ± 0.38, 1.54 ± 0.25, 0.80 ± 0.16, and 0.85 ± 0.11. Hepatic GLU uptake was 0.16 ± 0.06, 0.09 ± 0.05, 0,23 ± 0.06, and 0.43 ± 0.10 (p≤.05vsS). Net hepatic GLN balance was ‐0.06 ± 0.54, ‐0.77 ± 0.17, ‐0.21 ± 0.13, and 1.92 ± 0.39 (p≤.05 vs S).Conclusions:Neither hindlimb GLU uptake nor GLN release were influenced by nutrient infusion. Parenteral D blunted gut GLU release with no effect on gut GLN uptake. AA did not alter GLN or GLU balances in the organs measured. However, although AA+GLN infusion did not enhance gut GLN uptake, it did alter hepatic metabolism with a threefold increase in GLU uptake and a shift from net GLN equilibrium to GLN utilization. Thus, GLN administered parenterally after fasting was not directed preferentially for use by skeletal muscle or by gut tissues but rather was used extensively by the liver.(Journal of Parenteral and Enteral Nutrition20:25–30, 1996)